DISSERTATION ON

CLINICAL STUDY ON POSTERIOR UVEITIS

Submitted in partial fulfillment of requirements of

M.S.OPHTHALMOLOGY

BRANCH – III

REGIONAL INSTITUTE OF OPHTHALMOLOGY

MADRAS MEDICAL COLLEGE

CHENNAI – 600 003

THE TAMILNADU DR.M.G.R.MEDICAL UNIVERSITY,

CHENNAI

APRIL 2015

CERTIFICATE

This is to certify that this dissertation titled “A CLINICAL STUDY

ON POSTERIOR UVEITIS” is bonafide record of the research work

done by DR. KASTHURI. B,Post graduate in the Regional Institute of

Ophthalmology & Government Ophthalmic Hospital, Madras Medical

College and Government General Hospital, Chennai-03, in partial

fulfillment of the regulations laid down by the Tamil Nadu Dr. M.G.R

Medical University for the award of M.S. Ophthalmology Branch III,

under my guidance and supervision during the academic year 2012 – 2015.

PROF. DR.V. REVATHI M.S., D.O.,CHIEF, UVEA AND RETINA SERVICES,Regional Institute of Ophthalmology &Government Ophthalmic Hospital,Madras Medical College,Chennai-600 008.

PROF.DR.K.NAMITHABHUVANESWARI M.S., D.O.,DIRECTOR AND SUPERINTENDENT,Regional Institute of Ophthalmology &Government Ophthalmic Hospital,Madras Medical College,Chennai-600 008

PROF.DR.R.VIMALA.M.D.,DEAN

Madras Medical College &Government General Hospital,

Chennai-600 003.

DECLARATION BY THE CANDIDATE

I hereby declare this dissertation entitled “CLINICAL STUDY

ON POSTERIOR UVEITIS” is a bonafide and genuineresearch work

carried out by me under the guidance of Prof.Dr.V REVATHI, M.S D.O.,

DATE : DR.KASTHURI.B.

PLACE:

ACKNOWLEDGEMENT

I express my sincere thanks and gratitude to Prof.Dr.R.Vimala,

M.D., Dean, Madras Medical College, for permitting me to conduct this

study.

I have great pleasure in thanking Prof.Dr.K.Namitha

Bhuvaneswari, M.S., D.O.,Director and superintendent & The Head of the

Department of Cornea services, Regional Institute of Ophthalmology and

Government Ophthalmic Hospital, Madras Medical College, for her

valuable advice in preparing this dissertation.

I thank Prof.Dr.K.Vasantha M.S.,FRCS.,

Prof.Dr.K.Maragatham M.S.,D.O., and Prof.Dr.M.SRajarathinam

M.S.,D.O, former Directors of the RIOGOH for guiding me in my initial

stages at this institute and instilling an interest in the field of

Ophthalmology.

I express my profound gratitude to PROF.DR.V.Revathi.M.S.,

D.O., my unit chief and my guide for her valuable guidance and constant

support at every stage throughout the period of this study.

I am very grateful to my Co-guides, my unit assistant professors

DR.K.Ravikumar, M.S., and DR.P.Shobha,M.S. D.O., for rendering

their valuable advice and guidance for the study.

I am extremely thankful to my unit assistant professors,

DR.K.Rajasekar.M.S., DR.G.Balaji.M.S.D.O., DR.A.Samapapuri.M.S., &

DR.A.Nandhini.M.S for her valuable suggestions and guidance during the

course of this study.

I wish to express my sincere thanks to all the professors, assistant

professors and all my colleagues who had helped me in bringing out this

study.

Finally, I am indebted to all the patients for their sincere co-

operation for the completion of this study.

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CONTENTS

PART - I

S.NO CONTENT PAGE NO

1 INTRODUCTION 1

2 ANATOMY 2

3 HISTORICAL REVIEW 6

4 EPIDEMIOLOGY 8

5 PATHOGENESIS 10

6 CLINICAL MANIFESTATIONS 14

7 INVESTIGATIONS 39

8 TREATMENT 46

9 REVIEW OF LITERATURE 55

PART II

S.NO CONTENT PAGE NO

1 AIM AND OBJECTIVES OF THESTUDY

59

2 MATERIALS AND METHODS 60

3 RESULTS AND ANALYSIS 64

4 DISCUSSION 91

5 CONCLUSIONS 96

PART III

S.NO CONTENT

1 BIBLIOGRAPHY

2 PROFORMA

3 MASTER CHART

4 KEY TO MASTER CHART

5 ABBREVIATIONS

PART I

1

CLINICAL STUDY ON POSTERIOR UVEITIS

INTRODUCTION

Posterior Uveitis refers to inflammation of retina and or choroid.

Uvea the middle vascular coat of eye consists of iris, ciliary body and

choroid.

Posterior uveitis is less common than anterior uveitis.The

approximate incidence of 10 - 20 % can be extrapolated from the

literature.

Posterior uveitis with its varied aetiology, varied clinical picture,

associated multiple sequelae and complications signifies the early

diagnosis and prompt treatment. However the disease is associated with

frequent relapses and more protracted course often presenting a clinical

challenge to the treating Opthalmologist,as it is known for gradual

visual loss.

2

ANATOMY OF THE UVEAL TRACT

Uvea is the middle vascular coat of the eyeball, consists of iris,

ciliary body and choroid. The term uvea derived from latin word uva

(grape).

Iris

Iris is the anterior most part of the uveal tract and forms the

pupillary diaphragm of the eye. The anterior surface of iris is divided as

small pupillary zone and large peripheral ciliary zone by the collarette or

minor arterial circle, the thickest part of the iris7. The thinnest most

peripheral portion of the iris, iris root inserted to the middle of the

anterior surface of the ciliary body.

The microscopic structure of iris consists of anterior limiting

layer, iris stroma, anterior pigmented epithelial layer and posterior non

pigmented epithelial layer. Iris stroma consists of two smooth muscles

sphincter pupillae in the pupillary zone and dilator pupillae in the ciliary

zone.

3

Ciliary body

The ciliary body is the middle part of the uveal tract between iris

and choroid. Pars plicata (Corona ciliaris) containing finger like ciliary

processes is the anterior one third of ciliary body. Pars plana

(Orbicularis ciliaris) is the smooth posterior two thirds of ciliary body.

The microscopic structure consists of supra ciliary lamina, ciliary

body stroma, pigmented epithelial layer, non pigmented epithelial layer

and internal limiting membrane. Ciliary muscle is a non-striated muscle

consists of longitudinal,circular and radial fibres.

The major arterial circle located in the stroma of the ciliary body

and supplies iris, ciliary body and anterior choroid.

Choroid

The choroid is the posterior most part of the uvea that extends

from optic discto ora serrata between RPE and sclera. The microscopic

structure consists of suprachoroidal lamina,stroma, choriocapillaries and

bruch’s membrane .

The stroma consists of collagen, elastic and reticular fibres,

melanocytes, macrophages,mast cells, lymphocytes, plasma cells and

4

vessels arranged in two layers as outer layer of large vessels(Haller’s

layer), inner layer of medium vessels(Sattler’s layer) that supply and

drain choroid.

Choriocapillaries consists of a rich capillary network which

receives blood from large and medium vessels of stroma. Capillaries

contain fenestrated endothelial cells that allow passage of nutrients to

RPE and outer layers of sensory retina.

Bruch’s membrane (lamina vitrae) is the innermost layer of

choroid. It is a multilayered structure that lies between the

choriocapillaries and retinal pigment epithelium.

Vitreous Humour

It is a transparent gel that provides a clear optical medium,

structural integrity to the eye and a pathway for nutrients utilized by the

lens, ciliary body and retina. Vitreous is clear and avascular, filling the

space bound by the lens, retina and optic disc. It occupies approximately

80% of the globe volume. The vireous consists of largely of water

(99%), a network of collagen fibrils, hyaluronic acid, hyalocytes and

mucopolysaccharides, forming a gel like material.

5

Retina

It is the innermost layer of eyeball, a thin delicate and transparent

membrane. Retina extends from the optic disc to ora serrata. Grossly on

ophthalmoscopic examination it can be divided into three distinct

regions namely optic disc, macula lutea and peripheral retina.

Microscopic structure of retina consists of 3 types of cells (rods and

cones, bipolar cells, ganglion cells) and their synapses arranged in 10

layers.

Outer four layers of retina viz. retinal pigment epithelium, layers

of rods and cones, external limiting membrane and outer nuclear layer

get their nutrition from the choriocapillaries. Inner six layers get their

supply from the central retinal artery. The fovea is an avascular area

mainly supplied by the choriocapillaries. Inflammation of choroid

always involves the retina secondarily.

STRUCTURE OF IRIS

HISTOLOGY OF IRIS TRANSVERSE SECTION

STRUCTURE OF CHOROID AND RETINA

HISTOLOGY OF CHOROID

6

HISTORICAL REVIEW

1500 BC - Von Hippocrates mentioned the typical findings of

uveitis.

12th century - Mohammed-al-Ghafiqi described a disease with

poliosis, neuralgia and hearing changes.

19th century - Mackenzie described about poor vision after

couching for cataract in same eye and fellow eye

1650- 1730 - Antoine Maitre Jan described choroiditis for the first

time.

1881 - Von Michael emphasizedthe importance of

Tuberculosis in uveitis.

1900 - Neetleship considered a case of exudative choroiditis

to be due to dental infection.

1906 - Alfred Vogt and 1929 Koyanagi described bilateral

nontraumatic chronic iridocyclitis associated with

poliosis, vitiligo and dysacousia.

1926 - Harada described posterior uveitis with exudative

retinal detachment associated with CSF pleocytosis.

1924 - Shigeta in Japan, 1931- Adamantiades in French and

1937 – Hulsi Bechet reported a multisystem disorder

7

with triad of symptoms (recurrent ocular

inflammatory episodes, oral and genital leisons)

1936 - Sarcoid uveitis associated with facial nerve palsy and

uveoparotid fever was termed as Heerfordt’s

syndrome.

1940 - Brucellosis and Sarcoidosis were recognized as

clinical entities.

1946 - Allan C Wood considered that 75% of

granulomatous uveitis was due to Tuberculosis.

1950 - Toxoplasma uveitis became a proven infection, and

thus parasitic infection played a considerable role in

the aetiology particularly of posterior uveitis.

1950 - Wilder reported nematode larva in eyes enucleated

for retinoblastoma and Nichols determined the cause

is toxocara canis.

1952 - Helenor Campbell Wider identified the Toxoplasma

Gondii in eyes and confirmed it was the cause for

uveitis

1961 - Wood considered Histoplasmosis to be the cause of

13% of uveitic cases.

8

EPIDEMIOLOGY

The incidence of posterior uveitis is less common than anterior

uveitis. Infectious causes are more common in posterior uveitis.

Toxoplasmosis is the most common cause of infectious retinitis in

immunocompetent individuals. CMV retinitis is the most common

opportunistic ocular infection among AIDS patients.

Age incidence

Posterior uveitis can occur in all age groups. The etiology differs

in each age group. Toxocariasis, congenital Toxoplasmosis are common

in children. Toxoplasmosis, white dot syndromes and VKH syndrome

are common in 20-60years. Idiopathic retinal vasculitis and masquerade

syndromes occurin more than 60 years of age2.

Sex incidence

Males are more commonly affected in sympathetic ophthalmia,

Eales disease. Females are more affected in Rheumatoid Arthritis,

Systemic Lupus Erythematosus associated uveitis. There is no gender

predilection for infectious uveitis.

9

Duration and laterality

Majority of posterior uveitis is of chronic duration. Most cases of

posterior uveitis are bilateral. Parasitic diseases are typically unilateral.

10

PATHOGENESIS OF UVEITIS

a) Direct Bacterial invasion

One of the oldest and major hypothesis is the concept of direct

bacterial invasion. Another hypothesis for recurrent ocular inflammation

assumes a structural alteration within the eye resulting from a previous

inflammation that predisposes the to recurrent inflammatory episodes2.

b) Prostaglandins

Prostaglandin is a chemical mediator involved in the pathogenesis

of uveitis. Prostaglandin being synthesized by the enzyme prostaglandin

synthetase, cause a dramatic increase in protein content and flare of

aqueous humor and mild smooth muscle contraction (miosis).

c) The uvea as a node

When the antigen is introduced at distant site or is injected

directly into the circulation, antibody production begins inside the eye,

which takes up residence within the uvea and remain for long period.

Here the new antigen is needed to stimulate them for the renewal of the

antibody response.

11

d) Vitreous Antigen depot

Once antigen gain access to vitreous body,it tends to persist and

prolong immune responseto trapped antigen. Since hyalocytes have

macrophagic character, they may promote a persistent tendency to

recurrence of uveitis by processing antigen and modulating the immune

responses.

e) Focal infection

Any focal sepsis is predisposing factor for uveitis since most of

ocular inflammation are infective in nature. Among the foci of infection

the teeth is considered the most profile source. The others being the

tonsils, paranasal sinuses, respiratory tract, alimentary tract, uterus and

urinary tract.

f) Immune response

The major focus now is on the immune characteristics of the eye.

Absence of lymphatic drainage in the eye has special features and plays

a role in the Anterior Chamber Associated Immune Deviation (ACAID).

Uveitis wherein hypersensitivity is dominant, 3 types of reactions must

be considered.

12

1) Immediate Hypersensitivity (Anaphylaxis)

This results from contact of the uveal tissue to some foreign

protein namely bacterial protein, where an immediate antigen antibody

reaction occurs.

2) Delayed Hypersensitivity (Bacterial Allergy)

The tissues are sensitized by contact with living or dead organism

so that antibodies are formed on or within cells. Further contact with

same antigen causes severe cellular damage which develops slowly

causing an inflammatory and necrotic tissue reaction causing allergic

iridocyclitis.

3) Immune complex mediated disease

Immune complexes can be demonstrated in the aqueous of

patients with uveitis.e.g, Bechet’s disease. These findings have led to the

speculation that immune complex mediated tissue destruction could

explain intraocular inflammatory disease. Serum complement levels

have also been low in such patients.

13

g) Autoimmunity

It is an immune response directed against the host. Example is

autoantibody production to the lens. The presence of uveitogenic

antigens in the eye that are capable of inducing disease is an old concept

proposed as early as 1910 by Elschnig. The retina contains these

antigens (SAg) and it is also particularly prone to certain neurotropic

organisms like Toxoplasma Gondii and Herpes viruses.

h) Histo compatibility antigen of uveitis

HLA system is now regarded as the main leucocyte in antigen system.

Some special types of anterior uveitis has been associated with

inflammatory bowel disease like Ulcerative colitis, Crohn’s disaease, the

useful indicator being HLAB27. So there is considerable genetic

variability in susceptibility to the diseases.

14

CLASSIFICATION OF UVEITIS

Anatomical classification (IUSG)

Anterior uveitis - Iritis

- Iridocyclitis

- Anterior cyclitis

Intermediate uveitis - Posterior cyclitis

- Pars planitis

- Hyalitis

- Basal retinochoroiditis

Posterior uveitis - Choroiditis (focal/multifocal/diffuse)

- Chorioretinitis

- Retinochoroiditis

- Retinitis

- Neuroretinitis

- Retinal vasculitis

Panuveitis

15

Clinical classification

Laterality - Unilateral

- Bilateral

Severity - Mild

- Moderate

- Severe

Chronicity - Acute

- Acute recurrent

- Chronic

Pattern - Focal

- Multifocal

- Diffuse

Pathology - Granulomatous

- Non granulomatosus

Demographics - Age

- Sex

- Race

16

Aetiological classification

a) Exogenous uveitis : By external injury to the uvea or invasion of

microorganisms or other agents from outside.

b) Endogenous uveitis : By microorganisms or other agents from

within the patient.

17

POSTERIOR UVEITIS

Posterior uveitis is defined as intraocular inflammation primarily

involving retina and or choroid. In posterior uveitis inflammatory cells

may be observed diffusely through out vitreous cavity, overlying foci of

activeinflammation or in the posterior vitreous face. Macular edema,

retinal vasculitis and retinal or choroidal neovascularization are the

structural complications of posterior uveitis6.

Posterior uveitis encompasses

a) Retinitis

b) Choroiditis

c) Retinal vasculitis.

Retinitis

It may be focal, multifocal, geographic or diffuse. Active leisons

characterized by whitish retinal opacities with indistinct border due to

surrounding edema with overlying vitreous cells. As the lesion resolves

the borders become better defined.

18

Choroiditis

It may be focal, multifocal, geographic or diffuse. Active

choroiditis is characterized by a round yellow nodule. It does not usually

induce vitritis in the absence of concomitant retinal involvement. Old

inactive disease appear as atropic chorioretinal leisons with surrounding

hyperpigmentation.

Retinal Vasculitis

It may occur as a primary condition or as a secondary

phenomenon adjacent to a focus of retinitis. Veins are more commonly

involved than arteries. Active vasculitis is characterized by yellow or

grey white, patchy perivascular cuffing, retinal hemorrhages and cotton

wool spots. Quiescent vasculitis have perivascular scarring, atropic

retina and pigment epithelial stippling.

19

Aetiology of posterior uveitis

1) Non infectious causes

Collagen vascular diseases – Systemic Lupus Erythematosus,

Polyarteritis nodosa, Microscopic polyangitis and Wegener

granulomatosis.

2) Inflammatory chorioretinopathies of unknown etiology

Inflammatory chorioretinopathies or White dot syndromes are a

heterogenous group of inflammatory disorders with overlapping clinical

features. These include

a) Birdshot retinochoroidopathy

b) Acute posterior multifocal placoid pigment epitheliopathy

c) Serpiginous choroiditis

d) Multifocal choroiditis and panuveitis

e) Punctate inner choroiditis

f) Subretinal fibrosis and uveitis syndrome

g) Multiple evanescent white dot syndrome

20

h) Acute retinal pigment epithelitis

i) Acute zonal occult outer retinopathy

3) Infectious causes

a) Viral infections - Herpes simplex and Varicella zoster virus,

Cytomegalovirus, Epstein Barr virus, Rubella, Measles,

Lymphocytic choriomeningitis virus, Westnile virus, Rift

valley fever, Human T cell lymphotrophic virus, Dengue fever

and chikungunya fever

b) Bacterial infections – Tuberculosis, syphilis, Lyme disease,

Leptospirosis, Bartonellosis and Whipple disease

c) Fungal infections – Ocular histoplasmosis syndrome,

Candida, aspergillus and Cryptococcus

d) Protozoal infection – Toxoplasmosis

e) Helminthic infections – Toxocariasis, cysticercosis,

Onchocerciasis and Diffuse unilateral subacute neuroretinitis

4) Post traumatic uveitis

5) Post surgical uveitis

21

Symptoms of posterior uveitis

Floaters and defective vision are the most common symptoms of

posterior uveitis. Floaters result from the shadows cast by vitreous cells

and opacities on the retina.

Defective vision may be caused by the primary effects of uveitis,

such as retinitis or choroiditis directly affecting the macular function or

by the complications of inflammation such as cystoid macular edema,

epiretinal membrane,retinal ischemia,choroidal neovascularization,

opacities in the visual axis from inflammatory cells,fibrin, secondary

cataract, myopic or hyperopic shift from macular edema, protein in

anterior chamber and keratic precipitates inpanuveitis or spill over

anterior uveitis.

Symptoms due to anterior uveitis such as pain, redness,

photophobia, watering and decreased vision.

22

Signs of uveitis

In Anterior segment

Keratic precipitates

Inflammatorycells

Flare

Hypopyon

Pigment dispersion

Pupillary miosis

Iris nodules

Synechiae (anterior and posterior)

Band keratopathy (long standing cases)

23

SUN working group grading of Anterior Chamber cells

Cells in field Grade

<1 0

1-5 +-

6-15 1+

16-25 2+

26-50 3+

>50 4+

Grading of aqueous flare

Description Grade

Nil 0

Just detectable 1+

Moderate ( iris & lens details clear ) 2+

Marked ( iris & lens details hazy ) 3+

Intense ( fibrinous exudate ) 4+

24

Keratic precipitates (KPs)

These are small aggregates of inflammatory cells that accumulate

on the endothelial surface on cornea. It indicates current level of

inflammatory activity, mostly found in lower half of cornea in a base

down triangle configuration between 4 and 8’o clock position an area

termed as Arlt’s triangle2.

KPs are categorized on the basis of

Size - small / medium / large

Shape and colour - white and round (fresh)

- Shrunken and pigmented (old)

Appearance - mutton fat KPs (Granulomatous)

- White and round (Non granulomatous)

Perfield Grading

5-10 1+

11-20 2+

20-50 3+

>50 4+

25

Signs in posterior segment

Retinal or choroidal inflammatory infiltrate

Inflammatory sheathing of arteries or veins

Exudative, tractional or rhegmatogenous retinal detachment

Retinal pigment epithelial hypertrophy or atrophy

Swelling or atrophy of retina, choroid or optic nerve head

Preretinal or subretinal fibrosis

Retinal or choroidal neovascularization

Grading of vitreous cells ( Hruby lens )

Cells in

retroilluminated fieldDescription Grade

0-1 Clear 0+

2-20 Few opacities Trace

21-50 Scattered opacities 1+

51-100 Moderate opacities 2+

101-250 Many opacities 3+

>251 Dense opacities 4+

26

Examination of the anterior vitreous is done with a slit lamp by

rotating the slit 45 degrees and rotating the slit or illumination arm at the

minimum angle of separation from the viewing pathway.

Vitreous haze is a better indicator of active inflammation than are

vitreous cells because it combines the optical effect of cellular

infiltration and protein leakage. Grading of vitreous haze is done by

comparing the patient examination by indirect ophthalmoscope with

standard colour photograph in the examination room.

Grading of vitreous haze

Haze severity Grading

Good view of nerve fibre layer 0

Clear disc & vessels but hazy NFL 1+

Disc and vessels hazy 2+

Only disc visible 3+

Disc not visible 4+

27

Examination of Retina and Choroid

Examination of retina and choroid are done with combination of

indirect ophthalmoscope, Hruby lens, + 90 diopter lens, mirrored

contact lens. The indirect ophthalmoscope is ideal for defining the

extent and height of retinal and choroidal leisons, to find out peripheral

vascular sheathing, narrowing, obliteration and deep isolated choroidal

leisons. Hruby lens +90 diopter lens are useful to determine the depth of

the lesion. Mirrored contact lens are useful to look for the midperiphery

of retina.

28

Complications of posterior uveitis

Cystoid Macular edema (CME)

It is a common cause of visual loss in posterior uveitis . Macular

edema is caused by active intraocular inflammation that leading to

retinal vascular leakage and retinal pigment epithelial dysfunction. CME

is quantitatively evaluated and followed by serial spectral domain OCT

and Fundus Fluorescein Angiography.

A recent study of uveitic macular edema divided the edema

morphologically into diffuse macular edema, cystoid macular edema

and serous retinal detachment.

Retinal detachment

Rhegmetogenous retinal detachment and Tractional retinal

detachment are common in posterior uveitis. Infectious uveitis and

panuveitis are more frequently associated with rhegmatogenous retinal

detachment(RRD).Uveitis is usually still active with retinal detachment.

Upto 30% of patients with RRD may have proliferative

vitreoretinopathy at presentation. Repair is difficult due to preexisting

PVR, vitreous organization and poor visualization.

29

Vitreous opacification and Vitritis

Permanent vitreous opacification affects the vision. It is treated

with 3- port pars plana vitrectomy.

Proliferative retinopathy

Retinal neovascularization occurs from chronic inflammation or

capillary non perfusion. It is commonly seen in retinal vasculitis of

various causes and sarcoid panuveitis.

Choroidal neovascularization

Choroidal neovascularization results from a disruption of the

Bruch membrane from choroidal inflammation and the presence of

inflammatory cytokines that promote angiogenesis. It is commonly

occur in ocular Histoplassosis syndrome, puntate inner choroidopathy,

idiopathic multifocal choroiditis and serpiginous choroiditis. It can be of

foveal, juxta foveal, extrafoveal and peripapillary types.

Other complications due to spill over anterior uveitis

Secondary glaucoma

Complicated cataract

Hypotony

30

Aetiologyof posterior uveitis

Ocular Toxoplasmosis

Toxoplasmosis is the most common cause of infectious

retinochoroiditis in immunocompetent adults and children. Classically

presents as new unilateral white yellow retinal lesion with overlying

moderate vitreous inflammation (headlight in the fog), often adjacent to

a pigmented chorioretinal scar with perivasculitis and diffuse venous

sheathing of adjacent retinal vessels. Most of the leisons occurs in the

posterior pole.

Diagnosis is made clinically and serological evaluation using

ELISA test used to confirm the exposure to parasite. Treatment regimen

is classical triple therapy (systemic prednisolone, pyrimethamine and

sulfadiazine). Alternative regimens are co-trimaxozole or azithromycin

with systemic corticosteroids.

Tuberculosis

Uveitis is the most common manifestation of secondary ocular

TB. Tuberculous uveitis is classically a chronic granulomatous disease

that affect anterior and posterior segments.

31

Disseminated choroiditis is the most common presentation

characterized by deep, multiple, discrete, yellow leisons between 0.5

and 3 mm diameter located predominantly in posterior pole associated

with disc edema, vitritis, granulomatous anterior uveitis. Other

presentation single, focal, large, elevatedchoroidal mass (tuberculoma)

of 4-14 mm in size.

Other posterior segment findings of TB includes subretinal

abscess, CNV, optic neuritis and acute endophthalmitis. Retinal

involvement present as Eales disease and peripheral retinal

perivasculitis.

Cytomegalovirus retinitis

Cytomegalovirus is an opportunistic pathogen in

immunocompromised individuals and the most common infection in

AIDS typically occurs when the CD4 count is <50 cells/microliter.

Cytomegalovirus retinitis is characterized by greyish patches or

scaterred white dots with irregular sheathing of adjacent blood vessels.

There are superimposed haemorrhages followed by healing and retinal

atrophy. Ganciclovir is used in the treatment of CMV retinitis.

32

Toxocariasis

Ocular toxocariasis is an uncommon disease of children and

young adults that causes significant visual loss. It is acquired by

ingestion of soil containing eggs of the canine intestinal round worm

Toxocara canis. It otherwise involves healthy individualswith a normal

white cell count and absence of eosinophilia. It is unilateral and in

children it presents as chronic endophthalmitis and posterior pole

granuloma. In adolescence or adult life it presents as peripheral retinal

granuloma associated with a vitreous band extending to the disc or

macula causing visual impairment.

Lab diagnosis is by the high sensitivity and specificity (90%) of

an ELISA titre for Toxocara. Oral or periocular corticosteroids are used

for treatment.

Noninfectious autoimmune diseases

These are the collagen vascular diseases namely Systemic lupus

erythematotosus , Polyarteritis nodosa and Microscopic polyangitis and

Wegener granulomatosis.

33

Systemic lupus erythematosus

It is a connective tissue disorder with multisystem involvement

that primarily affects women of child bearing age. Ocular involvement

occur in 50% of cases and include cutaneous leisons on eyelids, sjogren

syndrome, scleritis, cranial nerve palsies and retinal vasculopathy.

Lupus retinopathy is an important marker of systemic disease

activity. The clinical spectrum is characterized by cotton wool spots

with or without intraretinal hemorrhages due to microangiopathy, severe

retinal vascular occlusive disease resulting in retinal nonperfusion and

ischemia, secondary retinal neovascularization and vitreous hemorrhage,

lupus choroidopathy resulting in serous elevations of retina, choroidal

infarction and choroidal neovascularization.

The diagnosis is essentially clinical based on revised diagnostic

criteria. Antinuclear antibody anti- ds DNA antibody (anti double

stranded deoxyribo nucleic acid antibody) and antiphospholipid

antibodies are positive in SLE.

Treatment is control of underlying disease with NSAIDS (Non

steroidal anti-inflammatory drugs), Corticosteroids and

34

immunosuppressive drugs. Ischemic complications are managed with

panretinal photocoagulation and vitrectomy surgery.

Polyarteritis nodosa and microscopic polyangitis

Polyartertis nodosa is an uncommon systemic vasculitis

characterized by subacute or chronic, focal,episodic necrotizing

inflammation of medium sized and small muscular arteries. It is seen in

patients between the ages of 40-60 years. Ocular involvement seen in

20% of patients includes hypertensive retinopathy, retinal arteriolar

occlusive disease, choroidal infarcts with exudative retinal detachment

secondary to vasculitis involving posterior ciliary arteries and choroidal

vessels, cranial nerve palsies and peripheral ulcerative keratitis with

scleral involvement. pANCA (perinuclear antineutrophil cytoplasmic

antibody)is positive in Polyarteritis nodosa and microscopic

polyangitis.Treatment consists of systemic corticosteroids and

immunomodulators6.

Wegener granulomatosis

It is a multisystem autoimmune disorder characterized by the

classic triad of necrotizing granulomatous vasculitis of upper and lower

respiratory tract, focal segmental glomerulonephritis and necrotizing

35

vasculitis of small arteries and veins. Ocular or orbital involvement seen

in 15% of cases. Orbital involvement is secondary to contiguous

extension of the granulomatous inflammatory process from the

paranasal sinuses.

Ocular involvement includes unilateral or bilateral anterior,

intermediate or posterior uveitis, with varying degrees of vitritis and

retinal vasculitis leading to retinal neovascularization, vitreous

hemorrhage and neovascular glaucoma. c ANCA (cytoplasmic

antineutrophil cytoplasmic antibody)positivity is sensitive and specific

for Wegener granulomatosis. Treatment includes systemic

corticosteroids and immunosupressants.

Eales disease

It is an idiopathic, inflammatory peripheral retinal vasculopathy

which presents with recurrent vitreous hemorrhages in young males. It

has been suggested that a hypersensitivity of retinal vessels to

tuberculoproteins may be the cause for retinal vasculitis. The vasculitis

leads to obliteration of affected vessels, subsequent hypoxia and

vasoproliferation.

36

It is clinically seen as sheathing of the vessels, which leaks

copiously on FFA. Hemorrhages , soft exudates and retinal edema are

common at the junction of perfused and non perfused zones of retina. In

proliferative stage it presents as recurrent vitreous hemorrhages, vitreous

traction and retinal detachment.

Treatment of acute vasculitic stage consists of systemic steroids.

Proliferative stage is treated with retinal photocoagulation and

vitreoretinal surgery.

White dot syndromes

The inflammatory chorioretinopathies or white dot syndromes are

a heterogenous group of inflammatory disorders with overlapping

clinical features that share in common the presence of discrete, multiple,

well circumscribed, yellow white leisons at the level of retina, outer

retina, RPE, choriocapillaries and choroid during some phase of their

course. These consists of predominantly non infectious ocular

syndromes.

Common presenting symptoms include photopsias, blurred vision,

nyctalopia, floaters and visual field loss contiguous with a blind spot.

The syndromes are bilateral and asymmetrical in nature. The etiology of

37

the white dot syndromes is unknown. Infectious, autoimmune and

infiammatory pathogenesis has been postulated for these disorders.

Panuveitis

Panuveitis is defined as inflammation involving all anatomical

compartment of eye (anterior chamber, vitreous and retina or choroid)

with no single predominant site of inflammation.It is usually bilateral.

Common causes are

a) Vogt – Koyanagi – Harada syndrome

b) Sarcoidosis

c) Sympathetic ophthalmia

d) Behcet disease

e) Infectious causes – Tuberculosis, Syphilis

Vogt –Koyanagi-Harada syndrome

It is an uncommon multisystem disease of presumed autoimmune

etiology that is characterized by chronic, bilateral, diffuse

granulomatous panuveitis with accompanying integumentary,

38

neurological and auditoryinvolvement. There are four stages of VKH

syndrome: prodromal, acute uveitic, convalescent and chronic recurrent.

Acute uveitic stage characterized by sequential blurring of vision

in both eyes with bilateral granulomatous anterior uveitis,variable

degree of vitritis, thickening of the posterior choroid, hyperemia and

edema of disc and multiple serous detachments. The chronic phase

shows diffuse RPE atrophy (sunset glow fundus).Complications include

CNV and subretinal fibrosis.

FFA of the acute phase shows multifocal hyperfluorescent dots at

the level of RPE and then accumulation of dye in the subretinal space.

The chronic phase shows are areas of hyperfluorescence due to RPE

window defects.

Treatment involves high dose oral prednisolone (60-100mg/day)

that may be augmented with 3 days intravenous pulse therapy with

methyl prednisolone (500-1000mg/day).Steroid resistant patients require

immunosupreesive therapy. Topical Corticosteroids and topical

cycloplegics for anterior uveitis.

39

INVESTIGATIONS

There is no one standardized battery of tests that need to be

ordered for all patients with posterior uveitis. Rather a tailored approach

should be taken based on the most likely causes for each patient. Once a

list of differential diagnosis is compiled appropriate laboratory tests can

be ordered. Many patients require only one or a few diagnostic tests6.

If the history and clinical examination do not clearly indicate any

cause, purified protein derivative skin test, chest radiograph, chest

computed tomography, serum angiotensin converting enzyme and

syphilis serologies are done to rule out the most common causes

(Tuberculosis, Syphilis and Sarcoidosis).

Laboratory tests and imaging studies with indications

Test Indications

HEMATOLOGICAL TESTS

Complete blood count Immunomodulator therapy

Erythrocyte sedimentation rate Gaint cell arteritis

Quatiferon gold Tuberculosis

T cell subsets AIDS

SEROLOGICAL TESTS Indications

40

Liver function test Immunomodulator therapy,

sarcoidosis

Renal function test Immunomodulator therapy

Angiotensin converting enzyme Sarcoidosis

Antiphospholipid antibodies Vascular occlusion

Rheumatoid Factor Rheumatoid arthritis, juvenile

idiopathic arthritis

Antinuclear antibody Connective tissue diseases

HLA testing

HLA-B27 Seronegative spondyloarthropathy

HLA-A29 Birdshot retinochoroidopathy

HLA-B51 Bechet disease

ANCA (c ANCA and p ANCA) Systemic vasculitides

VDRL/RPR Syphilis

FTA ABS Syphilis

Toxoplasma antibodies Toxoplasmosis

HSV,VZV,CMV serology Viral uveitis

HIV serology/ Westernblot HIV/AIDS

Radiographic studies Indications

Chest radiograph Tuberculosis, sarcoidosis, wegener

granulomatosis

Sacroiliac joint Ankylosing spondylitis

CT chest Sarcoidosis

CT/MRI brain and orbits Sarcoidosis, toxoplasmosis

41

Complete blood count and differential count

It is done to determine whether there isacute or chronic

inflammation. Complete blood count is obtained before initiating

systemic therapy with either corticosteroid or immunosuppressive drugs.

Erythrocyte sedimentation rate

It is a non-specific indicator of plasma fibrinogen and globulin

levels and may be elevated in systemic infection or inflammation or

malignancy. It is done using Westergren method.

Rheumatoid Factor

Rheumatoid Factor (RF) is an autoantibody directed against the

Fc fragment of human IgG. About 80% of Rheumatoid Arthritis patients

are RF seropositive, defined as a titre of more than 1:80. RF

seropositivity is non specific and best to support a clinical diagnosis of

Rheumatoid Arthritis.

Antinuclear Antibodies (ANA)

The ANA test is typically performed by applying serial dilutions

of the patients serum to cultured tumor cells and then titrating for the

presence and pattern of nuclear antibody staining. The ANA test is

42

generally used to confirm collagen vascular disease particularly

Systemic Lupus Erythematosus or Juvenile Rheumatoid Arthritis.

Herpes Virus antibodies

The prevalence of Herpes virus antibodies is so high in the

general population that a positive antibody titre is virtually meaningless.

A negative titre , however eliminates herpes infection and therefore can

be useful in selected instances.Herpes virus serology should remain

positive for life.

HIV antibodies

Most commonly detected by using an Enzyme Linked Immuno

Sorbent Assay (ELISA), positive results are confirmed by a westernblot

test. HIV testing in uveitis is usually orderedin patients with known HIV

risk factors, severe or bilateral retinitis or choroiditis. HIV testing

requires patient consent.

Toxoplasma antibodies

Tests available to detect and quantify antitoxoplasma gondi

antibodies are sabin Feldman dye test(SF), Immuno Fluorescence

Antibody (IFA) test and ELISA. Of these SF dye test remains the most

43

sensitive and specificbut it is technically difficult and of limited

availability, where as IFA ana ELISA are relatively easy and

economical and can be used to distinguish IgG and IgM anti

Toxoplasma gondii antibodies. When interpreting positive titres, it is

important to remember that IgM anti Toxoplasma antibodies may be

elevated for upto 1 year after infection, limiting the accuracy with which

they can date acute infection and that antibody titres are generally less

reliable in patients with AIDS.

Angiotensin Converting Enzyme level (ACE)

ACE is produced primarily by capillary endothelial cells,

abundant in both lungs and liver, and by macrophages. Clinically, ACE

levels are elevated in more than two thirds of patients with a active

disease of sarcoidosis.

Uveitis and negative Purified Protein Derivative (PPD) with

increased ACE is fairly specific for sarcoidosis. Normal serum ACE

level is 12-55mol/min/ml in men and 11-19 mol/min/ml in women.

Human Leucocyte Antigen (HLA) study

The surface membrane of human leucocyte contain HLA. These

are regulated by gene loci on chromosome 6. The reaction of these

44

antigens with specific antisera cause lysis of the cell membrane and this

is the basis of cell typing. HLAB27 has been associated with

Ankylosing spondylitis and Reiter’s syndrome.

Mantoux test

Purified protein derivative of tuberculin is injected intradermally.

It is a non-specific test. Because of prior exposure to tuberculosis, a

large number(8 to 30%) of healthy adults have positive PPD skin test

representing inactive infection. Therefore it is disadvantageous as it

yields more false positive than true positive results.

X ray chest and X ray sacroiliac joints

Chest x ray is taken in patients suspected by having sarcoidosis or

tuberculosis. X ray sacroiliac joints is taken in patients also complaints

of joint pains and hip pains.

Fundus Fluorescein angiography

It is an essential modality for evaluation of posterior uveitis. It is

useful for both diagnosis and monitoring patient’s response to therapy.

Areas of choroidal, retinal and optic nerve inflammation, cystoid

45

macular edema, retinal vasculitis, secondary choroidal and retinal

neovascularization are detected angiographically.

Ultrasonography

It is useful in demonstrating vitreous opacities, choroidal

thickening, retinal detachment or cyclitic membrane formation,

particularly if media opacities preclude a view of posterior segment6.

Optical coherence tomography

It is used for the objective measurement of uveitic cystoid

macular edema, retinal thickening, subretinal fluid associated with

choroidal neovascularization and serous retinal detachment.

Indocyanine green angiography

It shows 2 patterns of hypofluorescence in inflammatory

choroidal vasculopathies. Type 1 in inflammatorychoriocapillaropathies

demonstrate early and late multifocal areas of hypofluorescence. Type 2

represents stromal inflammatory vasculopathies of choroid and

demonstrates areas of early hypofluorescence and late

hyperfluorescence.

46

TREATMENT

Mydriatic and Cycloplegic agents

Topical mydriatic and cycloplegic agents are beneficial for

breaking or preventing theformation of posterior synechiae and for

relieving photophobia secondary to ciliary spasm in spill over anterior

uveitis or panuveitis. The stronger the inflammation, the stronger or

more frequent the dose of cycloplegic. Short acting drugs such as

cyclopentalate hydrochloride 1% or long acting drops such as atropine

0.1% may be used.

Corticosteroids

Corticosteroids are the mainstay of posterior uveitis therapy. It

may given in topical, periocular or systemic routes.

Topical steroids

Topical steroids are effective primarily for anterior uveitis. 1%

prednisolone acetate eye drops started as hourly, once the inflammation

is controlled , frequency gradually tapered to 2 hourly, 3 hourly then 4

times a day, eventually reduced by one drop a week until it reaches one

drop day. The drops discontinued within 5- 6 weeks. Complications are

47

elevation of IOP, cataract and uncommon complications are secondary

corneal infection, cornea melting.

Periocular steroids

Periocular steroids are given as first line therapy to control

inflammation and macular edema in unilateral posterior uveitis, to

supplement systemic therapy or when systemic steroids are

contraindicated in bilateral posterior uveitis. It delivers a therapeutic

dose of medication close to site of inflammation. Triamcinolone

acetonide (40mg) or methylprednisolone acetate (40-80mg) are most

commonly used drugs.

Periocular injections can be given through transseptal or subtenon

(Nozik technique) approach either in superotemporal (preferred) or

inferotemporal quadrant. Patient is instructed to look down and nasally,

after anesthesia is applied with a cotton swab soaked in proparacaine ,

needle is placed bevel down against the sclera and advanced through

the conjunctiva and tenon capsule using side to side movement upto the

hub,then drug is injected into the subtenon space.

Complications are ptosis, globe perforation, periorbital or

retrobulbar hemorrhage, orbital fat atrophy, skin discoloration

48

andelevation of IOP for long time. Periocular injections are

contraindicated in infectious posterior uveitis.

Systemic corticosteroids

Systemic steroids are used in vision threatening posterior uveitis,

panuveitis or when systemic disease also requires therapy. Prednisolone

is the most commonly used drug. Start with a large dose and then

reduce. The starting dose of prednisolone 1-2mg/kg/ day given in a

single morning dose after breakfast. A high level is maintained until a

clinical effect is seen followed by a slow taper over every 1-2 weeks

until the disease is quiescent. The lowest possible dose that will control

inflammation and minimize side effects is desired. This dose should be

5-10mg/day. If dose greater than this is required or treatment required

for longer than 3 months, steroid sparing immunomodulator therapy is

indicated.

In explosive onset of severe non infectious posterior uveitis or

panuveitis intravenous high dose pulse methylprednisolone (1g/day

infused over 1 hour) therapy may be administered for 3 days followed

by a gradual taper of oral prednisolone.

49

Side effects of short term therapy includes dyspepsia, mental

changes, electrolyte imbalance and aseptic necrosis of the head of

femur. Side effects of long term therapy includes cushingoid state,

osteoporosis, reactivation of infections, cataract and exacerbation of

diabetes and myopathy.

Contraindications are poorly controlled diabetes, peptic ulcer,

osteoporosis, active systemic infection, psychosis on previous exposure

to steroids.

Intravitreal administration

1) Intravitreal injections

2) Intravitreal implants

Intravitreal injection of preservative free triamcinolone acetonide

through single trans pars plana route, 4mg/0.1ml given for recalcitrant

uveitic cystoid macular edema and choroidal neovascularization. It

produces sustained improvement in visual acuity for 3-6 months.

Intravitreal sustained release implants (fluocinolone acetonide

0.59mg, dexamethasone-ozurdex 350/700 microgram) are given for non

infectious posterior uveitis. Early post operative complications are

50

endophthalmitis, wound leak, vitreous detachment and retinal

detachment.Cataract and secondary glaucoma are the late common

complications2.

Immunomodulators

Antimetabolites, inhibitors of T cell signaling, alkylating agents

and biological response modifiers are the commonly used

immunomodulators.

Indications for immunomodulators in posterior uveitis are

Severe vision threatening posterior uveitis

Patients resistant to or cannot tolerate corticosteroids,

When corticosteroids are contraindicated due to systemic

problems

Patient requires chronic corticosteroid therapy (longer than 3

months) at doses greater than 5-10 mg/day

Chronic topical corticosteroid dependence and those who

requiring multiple periocular corticosteroid injections.

51

Corticosteroids are the mainstay of initial therapy, but early use of

immunomodulator therapy is indicated in certain specific uveitis

(Serpiginous choroiditis, VKH, Bechets disease and

sympatheticophthalmia) to improve the long term prognosis and tovisual

morbidity. Before initiating the therapy, infections, hepatic and

hematologic contraindications should be ruled out.

Therapeutic effect of immunomodulators will start only after

several weeks. So patients should be maintainedon corticosteroids until

the immunomodulators begin to take effect, at that timecorticosteroid

dose gradually tapered.

Immunomodulatory drugs in posterior uveitis

Medications Dosage Complications

Antimetabolites

Methotrexate 7.5-25

microgram/week

Hepatotoxicity, GI upset

Azathioprine 100-250mg/day Hepatotoxicity, GI upset

Mycophenalate

mofetil

1-3 g/day GI ulceration, diarrhea

Inhibitors of T cell

signaling

52

Cyclosporine 2.5-5mg/kg/day Nephrotoxicity,hypertension

Tacrolimus 0.1-0.2mg/kg/day Nephrotoxicity,hypertension

Sirolimus 6mg iv loading

dose, 4mg/day iv

increased by 2mg

increments

GI upset

Alkylating agents

Cyclophosphamide 1-2mg/day Hemorrhagic cystitis, sterility

Chlorambucil 2-12mg/day Hemorrhagic cystitis, sterility

Biological

response modifiers

Infliximab 3mg/kg iv 0,2,6

weeks then once

in 6-8weeks

Infusion reactions, infections,

malignancy

Adalimumab 40mg/week Headache, GI upset

Daclizumab 1mg/kg iv once in

two weeks 5 doses

Rituximab Two doses 1g iv

two weeks apart

Late onset neutropenia

Complications include hepatic and renal toxicity, bone marrow

suppression and increased susceptibility to infections. Patients should be

monitored with complete blood count, liver and renal function test

53

regularly. These agents are teratogenic, so patients should be advised to

avoid pregnancy during treatment.

Treatment of Infectious posterior uveitis

Infectious posterior uveitis is treated with systemic antimicrobial

drugs and systemic corticosteroids. Antibiotics, antiviral drugs,

antifungal drugs, anti parasitic agents are the antimicrobial drugs used in

posterior uveitis. The choice of antimicrobials depends on the etiology

of posterior uveitis.

Treatment of sequelae and complications

Secondary glaucoma is treated with antiglaucoma medications.

Topical corticosteroids and aqueous suppressants are administered

topically and acetazolamide is given systemically. Pilocarpine and

prostaglandin analogues are contraindicated in uveitic glaucoma.

Cataract are removed surgically after uveitis is quiescent for

atleast 2-3 months. Cystoid macular edema is treated with meticulous

control of intraocular inflammation with corticosteroids,

immunomodulator drugs and periocular steroids.

54

Proliferative retinopathy is treated with laser photocoagulation.

Permanent vitreous opacification affecting vision is treated with 3– port

pars plana vitrectomy. Rhegmatogenous retinal detachment is treated

with scleral buckling with cryoretinopexy, pars plana vitrectomy and

endolaser with silicone oil tamponade or combined scleral buckling and

pars plana vitrectomy. But the prognosis is poor . Retinal and Choroidal

neovascularization are treated with control of inflammation using

corticosteroids and immunomodulators, focal laser photocoagulation

and intravitreal injectionof bevacizumab.

In spite of all treatment modalities 10% patients will develop

permanent loss of vision. More so the patients with systemic association

of diseases, treatment of posterior uveitis and restoration of vision is a

challenge to all Ophthalmologists.

55

REVIEW OF LITERATURE

Ocular toxoplasmosis is one of the most common type of

Posterior uveitis of infectious origin comprising 30- 50% of

cases. Pyrimethamine and sulfadiazine with corticosteroids is the

classical chemotherapy most widely used in the treatment for

ocular toxoplasmosis. An alternative treatment with

Trimethoprim/sulfamethoxazole plus oral prednisolone showed

to have similar efficacy to classical therapy (de-la-Torre A et al

Therapy for ocular toxoplasmosis. Ocul Immunol Inflamm.

2011;19:314–320)8.

In a study conducted by Anna Elias et a, the mean age

presentation of VKH Syndrome was 37.26 years. Majority of

patients had exudative retinal detachment, followed by optic dis

edema and anterior uveitis. Fundus fluorescein angiography

(FFA)showed multiple pinpoint hyperfluorescent leaks at the

level of the retinal pigment epithelium in all patients. All patients

were treated with systemic steroids. 17.39% patients were also

treated with immunosuppressants. 5.26% patients developed

subretinal fibrosis and 5.26% patients developed secondary

56

glaucoma 89.47% had a final visual acuity better than 6/12.The

eyes with secondary glaucoma responded to topical anti-

glaucoma meditations.

The more common manifestation of ocular tuberculosis is chronic

granulomatous iridocyclitis with multifocal posterior choroiditis.

Choroidal granuloma is an atypical presentation for ocular

tuberculosis and is less commonly reported.Patients are treated

with category I ATT for total 6 months duration and Choroidal

nodular lesion will resolve completely after 8 weeks of starting

Anti-tubercular chemotherapy, with BCVA improving to 20/20.

(Laurent J et al Arch Ophthalmol. 2005;123:864-866 )19.

The most frequent clinical presentation of Eales' disease is a

sudden painless loss of vision because of vitreous hemorrhage.

Corticosteroids remain the mainstay of the treatment in the active

perivasculitis stage of Eales' disease. Laser photocoagulation is

the mainstay of treatment in the proliferative stage of Eales'

disease. Fluorescein angiography helps in monitoring the

response to treatment. (Abu El-Asrar and Al-Kharashi Br J

Ophthalmol 86:1248-1251)23.

57

Serpiginous choroidopathy occur typically at the disc and spread

in a helicoid pattern along the major vascular arcades towards the

macula.Combination azathioprine and systemic corticosteroids is

a safe and acceptable treatment . Recurrences are common and

manifest as yellow-grey extensions at the level of the

choriocapillaris, contiguous or as satellites to existing areas of

chorioretinal atrophy . Visual disability may result directly from

retinal lesions affecting the central macula, or from secondary

choroidal neovascularization (Jampol LM et al Am J Ophthalmol

88:683–689).

CMV retinitis is one of the most common complications of AIDS

patients, it can affect 6 to 38% of patients and may be bilateral in

30 to 50% with up to 25% of the affected patients possibly losing

their vision ( Holland GN, et al . American Journal of

Ophthalmology, 114: 86-95).

Ocular toxocariasis is relatively uncommon,occurring in1% of

uveitis. Clinical presentation is unilateral (90.9%). Ocular

Toxocarasis is characterized by a granuloma in the peripheral

retina in 50% of cases, granuloma in the macula in 25% of cases,

and severe vitreous inflammation mimicking endophthalmitis in

58

25% cases. The primary causes of poor vision are cystoid

macular edema (47.4%), and traction retinal detachment (36.8%).

The mainstay of treatment of Toxocariasis is corticosteroids to

reduce inflammatory responses (Smith H et al Trends Parasitol

25: 182–188. doi: 10.1016/j.pt.2009.01.006) .

Ocular manifestations in SLE may be vision threatening and is

indicator of active systemic disease. The mainstay of treatment is

systemic corticosteroids and immunosuppressive

drugs.Proliferative retinopathy is treated with panretinal

photocoagulation Giorgi D et al.

PART II

59

AIM OF THE STUDY

To analyse the posterior uveitis with reference to age and sex

incidence, laterality, etiology, chronicity, severity, clinical presentation,

sequelae, complication and treatment modalities.

Primary objective

• To evaluate the various etiological factors and predisposing

factors leading on to posterior uveitis.

• To assess the clinical presentation in different types of posterior

uveitis.

• To diagnose and start treatment after systematic evaluation

Secondary objective

• To assess visual outcome after treatment of Posterior Uveitis

since Posterior uveitis treatment is a challenge to all

Ophthalmologists.

60

MATERIALS AND METHODS

The study design was a prospective study of 30 patients with age

range of 20-45 years with posterior uveitis, conducted in Regional

Institute of Ophthalmology and Ophthalmic Eye Hospital during August

2013 to August 2014 for a period of 12 months.

Main criteria for diagnosis

1) Patients having whitish retinal opacities with indistinct borders

(focal/multifocal/diffuse) and vitritis suggestive of retinitis

2) Patients having round yellowish nodule in the fundus

(focal/multifocal/diffuse) suggestive of choroiditis

3) Patients having yellow or grey white, patchy perivascular cuffing

suggestive of active vasculitis

4) Patients having papillitis with multiple serous detachment

suggestive of VKH syndrome

5) Patients having peripheral tubercles

SLIT LAMP EXAMINATION

KERATIC PRECIPITATES

ACTIVE CHOROIDITIS ADJACENT TO PIGMENTED CHORIORETINAL SCAR

HEAD LIGHT IN THE FOG APPEARANCE

61

Exclusion criteria

1) Post surgical cases

2) Post trauma cases

3) Intermediate uveitis ( predominant vitritis without active

chorioretinal lesion)

4) Predominant anterior segment involvement without active

chorioretinal lesion)

5) Patients who lost follow up.

All these patients were questioned about thepresenting compliants

(floaters, defective vision), history of contact with pets, tuberculosis,

joint pain and focal sepsis.

Systemic examination of cardiac, pulmonary, gastrointestinal,

central nervous system and musculoskeletal system was done.

Complete ocular examination including visual acuity using

Snellen’s acuity chart, slit lamp examination of the anterior segment,

lens and vitreous, posterior segment examination with direct and indirect

62

ophthalmoscopy, slit lamp biomicroscopy using 90 diopter lens, intra

ocular pressure measurement were done.

All these patients were subjected to a battery of investigations

including total count, differential count, erythrocyte sedimentation rate,

chest x ray PA view, mantoux test and blood sugar. Further

investigations depends on probable etiology of posterior uveitis.

TORCH screening and Quantiferon gold were done in infectious cases.

Fundus fluorescein angiography was done in non infectious cases.

ANA, dsDNA antibody was done in suspected cases of systemic lupus

erythematosus. Optical coherent tomography was done in choroidal

neovascularization. CD4 count was done in suspected cytomegalovirus

infection. Liver function tests and renal function tests were done in

patients who required immunosuppressive therapy.

Patients were treated with topical and systemic corticosteroid

therapy in non-infectious posterior uveitis, systemic antimicrobials,

topical and systemic corticosteroids in infectious posterior uveitis

following which dose will be tapered over a period of 2 months.

Immunosuppressive therapy was given in patients not responding to

corticosteroids and those who required prolonged corticosteroid therapy.

63

Proliferative retinopathy was treated with panretinal

photocoagulation. Intravitreal injection bevacizumab was given for

choroidal neovascularization. Post inflammatory glaucoma was

managed with topical antiglaucoma medications.

All patients were followed up every week for 4 weeks, every two

weeks for one month then every month for 4 months, totally of 6

months.

Improvement in visual acuity, intra ocular pressure, resolution of

vitritis and choroidal leisons were assessed during follw up.

HEALED CHOROIDITIS

ACUTE VKH SYNDROME

CHRONIC VKH SYNDROME

FFA WINDOW DEFECTS IN VKH

64

RESULTS AND ANALYSIS

Table 1 : Age Distribution

Age GroupCases

No %

21 25 yrs 6 20

26 – 30 yrs 8 26.7

31 – 35 yrs 7 23.3

36 – 40 yrs 6 20

41 – 45 yrs 3 10.0

Total 30 100

Range 21 – 45 yrs

Mean 32.2 yrs

SD 6.3 yrs

In our study maximum number of cases posterior uveitis were

found to be within the age groups of 26-30 years and 31-35 years

comprising 26.7% and 23.3% respectively.

65

Table 2 : Sex Distribution

SexCases

No %

Male 14 46.7

Female 16 53.3

Total 30 100

Out of cases in our study 14 cases were males (46.7%), 16 cases

were females (53.3%). Not much of sexual predilection towards any

group in our study.

Table 3 : Laterality

LateralityCases

No %

Unilateral 15 50

Bilateral 15 50

Total 30 100

Regarding the laterality, out of 30 cases in our study 15 cases

(50%) were unilateral and 15 cases were bilateral (50%). The laterality

was equal in our study.

66

AGE DISTRIBUTION

5, 16%

9, 30%

8, 27%

5, 17%

3, 10%

21 - 25 yrs 26 - 30 yrs 31 - 35 yrs36 - 40 yrs 41 - 45 yrs

SEX DISTRIBUTION

14, 47%16, 53%

MALE

67

Table 4 : Duration and Onset

Duration No of cases Percentage

Acute 0 0

Acute recurrent 0 0

Chronic 30 100%

In our study out of 30 cases, all cases (100%) were of chronic

duration of more than 6 weeks. There was no acute and acute recurrent

cases.

Table 5: Severity of posterior uveitis

Severity No. of cases Percentage

Mild 0 0%

Moderate 0 0%

Severe 30 100%

In our study out of 30 cases, all cases (100%) were of severe in nature.

CMV RETINITIS

SERPIGINOUS CHOROIDOPATHY

CHOROIDAL TUBERCULOMA

BEFORE TREATMENT

AFTER TREATMENT

68

Table 6 : Aetiology of posterior uveitis

Aetiology No of cases Percentage

Infectious 18 60%

Non infectious 12 40%

Total 30 100%

In our study out of 30 cases, 18 cases (60%) were of infectious

etiology and 12 cases (40%) non infectious etiology. Infectious etiology

was more common than non infectious etiology in our study.

69

LATERALITY

15, 50%

15, 50%

UNILATERALBILATERAL

AETIOLOGY OF POSTERIOR UVEITIS

18, 60%

12, 40%

InfectiousNon Infectious

70

Table 7 : Aetiological Diagnosis

AetiologyCases

No %

Toxoplasmosis

a) Macular area

b) Extramacular area

c) Total

8

5

13

26.7

16.7

43.3

VKH Syndrome 5 16.7

Cytomegalovirus retinitis 3 10.0

SLE- Retinal Vasculitis 3 10.0

Serpiginous Choroidopathy 3 10.0

Eale’s disease 1 3.3

Tuberculosis 1 3.3

Toxocariasis 1 3.3

Total 30 100

In the aetiological analysis, 13 cases (43.3%) were of Toxoplasma

etiology, 5 cases (16.7%) of VKH Syndrome, 3 cases (10.0%) were of

serpiginous choroidopathy, 3 cases (10.0%) were of cytomegalovirus

retinitis, 3 cases (10.0%) were of SLE retinal vasculitis. Eale’s disease

was found in one case (3.3%), one case (3.3%) had Tuberculous

etiology and Toxocariasis was found in one case (3.3%).

71

AETIOLOGICAL DIAGNOSIS

ANATOMICAL CLASSIFICATION

0 10 20

Choroiditis

Retinochoroiditis

Chorioretinitis

Retinal Vasculitis

Panuveitis

216

3

4

5

Number of cases

0 5 10 15 20 25 30

Macular area Toxoplasmosis

Extramacular areaToxoplasmosis

VKH Syndrome

Cytomegalovirus retinitis

SLE- Retinal Vasculitis

SerpiginousChoroidopathy

Others

26.716.7

16.7

1010

10

10

Percentage of cases

72

Table 8 :Anatomical classification

Anatomical

Classification

Cases

No %

Choroiditis 2 6.7

Retinochoroiditis 16 53.3

Chorioretinitis 3 10.0

Retinal Vasculitis 4 13.3

Panuveitis 5 16.7

Total 30 100

Based on anatomical classification of Posterior uveitis in our

study, 16 cases (53.3%) of cases were Retinochoroiditis, 4 cases

(13.3%) were Retinal vasculitis, 3 cases (10.0%) were Chorioretinitis, 2

cases (6.7%) were Choroiditis and 5 cases (16.7%) were found to be

Panuveitis.

73

Table 9 : Aetiological analysis based Anatomical classification.

AetiologyChoroditis

Retina

choroditis

Chorio

Retinitis

Retinal

VasculitisPanuveitis

No % No % No % No % No %

Toxoplasmosis

(13)- - 13 81.25 - - - - - -

VKH Syndrome

(5)- - - - - - - - 5 100

Serpiginous

Choroidopathy

(3)

- - - - 3 100 - - - -

SLE-Retinal

Vasculitis (3)- - - - - - 3 75 - -

Cytomegalovirus

retinitis (3)- - 3 18.75 - - - - - -

Eale’s disease

(1)- - - - - - 1 25 - -

Tuberculosis (1) 1 50 - - - - - - - -

Toxocariasis (1) 1 50 - - - - - - - -

In case of Choroiditis only 2 cases were present in our study in

that one was Tuberculosis another was Toxocariasis. In

Retinochoroiditis 81.25% of cases were Toxoplasmosis and 18.75% of

cases were Cytomegalovirus infection. In retinal vasculitis 75% were

74

due to systemic lupus erythematosus and 25% was due to Eale’s disease.

Panuveitis is mainly due to VKH Syndrome (100%).

In our study choroiditis and chorioretinitis were of infectious

origin. Retinal vasculitis was due to SLE and Eales disease.

75

Table 10 :Age incidence based on anatomical classification

Age

No

of

cases

ChoroditisRetina

choroditis

Chorio

Retinitis

Retinal

VasculitisPanuveitis

No % No % No % No % No %

21 - 25 6 1 16.7 4 66.7 - - 1 16.7 - -

26 - 30 8 - - 4 50 - - 2 25 2 25

31 - 35 7 -- - 4 57.1 - - 1 14.3 2 28.6

36 - 40 6 - - 3 50 2 33.3 - - 1 16.7

41 - 45 3 1 33.3 1 33.3 1 33.3 - - - -

Total 30 2 6.7 16 53.3 3 10.0 4 13.3 5 16.7

In our study maximum number of cases posterior uveitis were

found to be within the age groups of 26-30 years and 31-35 years

comprising 26.7% and 23.3% respectively. Age group affected in our

study was between 21- 45 years of age.

76

Table 11 :Sex incidence based on anatomical classification.

SexChoroditis

Retina

choroditis

Chorio

Retinitis

Retinal

VasculitisPanuveitis

No % No % No % No % No %

Male 1 50 8 50 3 100 1 25 2 40

Female 1 50 8 50 - - 3 75 3 60

In Choroiditis one case(50%) was male and one case (50%) was

female. In Retinochoroiditis 8 cases (50%) were males and 8 cases

(50%) were females. In Chorioretinitis all cases (100%) were males. In

Retinal vasculitis one case (25%) was male and 3 cases (75%) were

females. In Panuveitis 2cases (40%) and 3 cases (60%) were females.

77

Table 12 :Laterality based on anatomic classification

LateralityChoroditis

Retina

choroditis

Chorio

Retinitis

Retinal

Vasculitis

Pan

uveitis

No % No % No % No % No %

Unilateral 2 100 13 81.25 - - - - - -

Bilateral - - 3 18.75 3 100 4 100 5 100

Based on anatomical classification, all cases of Choroiditis were

unilateral. In Retinochoroiditis 13 cases (81.25%) were unilateral and 3

cases (18.75%) were bilateral. In Chorioretinitis all cases were bilateral.

In Retinal vasculitis all cases were bilateral. All cases of Panuveitis were

bilateral. Bilateral retinochoroiditis were due to CMV retinitis.

78

Table 13 : Vitreous

Vitreous No of cases Percentage

Normal 7 23.3

Grade I vitreous haze 8 26.6

Grade II vitreous haze 1 3.3

Grade III vitreous haze 13 43.3

Grade IV vitreous haze 0 0

Vitreous hemorrhage 1 3.3

Total 30 100

In our study out of 30 cases, grade III vitritis was seen in 13 cases

(43.3%), grade I vitritis was seen in 8 cases (26.6%),grade II vitritis was

seen in 1 case (3.3%). Vitreous hemorrhage was seen in one case (3.3%)

and vitreous was normal in 7 cases (23.3%). Majority of cases in our

study were presented with grade III vitritis.

79

Table 14 : Investigations

InvestigationsCases

No %

TORCH Screening, TC, DC, ESR, 17 56.7

FFA, RFT, LFT 12 40.0

Chest X Ray, Mantoux test 1 3.3

Quantiferon Gold 1 3.3

OCT 1 3.3

CD4 Count 3 10.0

ANA, anti ds DNA Antibody, RF, cANCA,

pANCA3 10.0

In our study most common investigation required was TORCH

screening,TC, DC and ESR for 17 cases (56.7%), followed by Fundus

Fluorescein Angiography, RFT and LFT for 12 cases (40%), CD4 count

for 3 cases (10%). Other investigations, Chest X Ray, Mantoux test,

ANA, anti ds DNA Antibody, RF, cANCA, pANCA, Quantiferon Gold

and OCT were required in one case (3.3%).

80

VITREOUS HAZE

7, 23%

8, 27%1, 3%

1, 3%13, 44%

Normal Grade I Vitreous hazeGrade II Vitreous haze Grade III Vitreous hazeVitreous Hemorrhage

INVESTIGATIONS

0 10

Torch Screening

FFA

CD4 Count

ANA / ds, DNA…Others

12333

81

Table 15 : Treatment

TreatmentCases

No %

Systemic corticosteroids 27 90

Topical mydriatics and cycloplegics 17 56.7

Topical corticosteroids 17 56.7

Anti Toxoplasma agents 13 43.3

Immunosuppressive drugs 11 36.66

Anti cytomegalovirus drugs 3 10.0

Panretinal photocoagulation 3 10.0

Anti tubercular drugs 1 3.3

Intra vitreal injection Bevacizumab 1 3.3

Anti glaucoma medications 1 3.3

In our study most common drugs used for treatment were

systemic corticosteroids, required in 27 cases (90%), followed by topical

corticosteroids, topical mydriatics and cycloplegics in 17 cases(56.7%).

Anti Toxoplasma agents were needed in 13 cases (43.3%) and

82

Immunosuppressive drugs were needed in 11 cases (36.66%). Anti

cytomegalovirus drugs and panretinal photocoagulation were given for 3

cases (10%).

Other treatments like Anti tubercular drugs, Intra vitreal injection

Bevacizumab and Anti glaucoma medications were given in one case

(3.3%).

83

Table 16 : Complications

ComplicationsCases

No %

Cataract 4 13.3

Glaucoma 1 3.3

Proliferative Retinopathy 3 10.0

Retinal Detachment 1 3.3

Subretinal Fibrosis 1 3.3

Choroidal

Neovascularization1 3.3

In our study, out of 30 cases of posterior uveitis, cataract was seen

in 4 cases(13.3%), proliferative retinopathy in 3 cases(10%), subretinal

fibrosis and choroidal neovascularization were seen in one case (3.3%).

Post inflammatory glaucoma was seen in one case (3.3%).

84

COMPLICATIONS

85

Table 17 : Visual outcome

Visual improvement No. of cases Percentage

6/6 3 10%

6/12 – 6/9 5 16.66%

4/60 – 6/36 20 66.66%

No improvement 2 6.66%

In our study of 30 cases, even with early diagnosis and prompt

treatment only in 3 cases (10%) vision improved to 6/6 and 5 cases

(16.66%) improved to 6/12 to 6/9. In remaining 20 cases (66.66%) there

was some visual improvement that is not very significant and in 2 cases

(6.66%) there was no visual improvement.

86

Table 18 : Visual Outcome based on aetiological diagnosis

DiseaseDisease

Contained

No

of

cases

Visual Outcome

RemarksVisual

ImprovementPre

Treatment

Post

Treatment

Toxoplasmosis Yes

5 6/36– 6/24 6/12 – 6/9Extra Macular

area

Improved

81/2/60–

2/606/60– 6/36

Macular

involvement

Improved

VKH Syndrome Yes

3 HM – 6/36 6/12 – 6/6 -Improved

1 1/60 1/60Choroidal

neovascularization

Not Improved

1 3/60 6/24Subretional

fibrosis

Improved

Cytomegalovirus

retinitisYes 3 HM – 3/60

4/60 –

6/60

Macular

involvement

Improved

Serpiginous

ChoroidopathyYes 3

4/60 –

6/36

6/36 –

6/12

Chorioretinal

atrophy

Improved

SLE – retinal

VasculitisYes 3

1/60 –

4/60

6/60 –

6/36

Proliferative

retinopathy

Improved

Eale’s disease Yes 1 HM 6/24Proliferative

Retinopathy

Improved

Tuberculosis Yes 1 1/60 6/36 -Improved

Toxocariasis Yes 1 3/60 1/60Tractional Retinal

Detachment

Not Improved

87

In our study out of 13 cases of Toxoplasmosis, 5 cases were

involved the extramacular area with good visual outcome , vision

improved to 6/12 to 6/9. 8 cases were showed macular involvement with

less improvement in vision in the range of 6/60 to6/36.

In VKH Syndrome, out of 5 cases 3 cases were improved vision

significantly 6/9 to 6/6. One case had subretinal fibrosis in macular area

with vision improving to 6/24. In one case was not improved due to

choroidal neovascularization.

In cytomegalovirus infection there was only mild improvement

in vision (4/60 to6/60) due to macular involvement. In serpiginous

choroidopathy visual outcome was affected by chorioretinal atrophy in

macular area, improved upto 6/36 to 6/12.

In Retinal vasculitis due to SLE (6/60 to 6/36) and in Eales

disease (6/24)visual outcome was affected by proliferative retinopathy.

In tuberculosis vision was improved to 6/36 and no complications.

In Toxocariasis vision was not improved (1/60) due to

development of tractional retinal detachment.

88

Table:19 Cause for poor visual outcome

Cause No. of cases Percentage

Chorioratinal atrophy

in macula

14 46.66%

Proliferative

retinopathy

3 10%

CNVM 1 3.33%

Sub retinal fibrosis 1 3.33%

Tractional Retinal

Detachment

1 3.33%

In our study, the most common cause for poor visual outcome is

chorioretinal atrophy (46.66%) seen in 14 cases followed by

proliferative retinopathy seen in 3 cases (10%). Others were CNVM,

subretinal fibrosis and tractional retinal detachment seen in 3.33% of

cases.

89

Table 20 : Sequelae and Complications

Pathology Remarks No. of cases percentage

Structural

damage

Chorioretinal

atrophy

14 46.66%

Complication CNVM,

subretinal

fibrosis,

tractional retinal

detachment,

proliferative

retinopathy

6 20%

In our study, poor visual outcome due to structural damage (

chorioretinal atrophy) seen in 14 cases (46.66%) and due to

complications were (20%)

In our study, Structural damage caused by the disease was more

common than the complications.

90

Statistical Tools

The information collected regarding all the selected cases were

recorded in a Master Chart. Data analysis was done with the help of

computer using Epidemiological Information Package (EPI 2010)

developed by Centre for Disease Control, Atlanta.

Using this software range, frequencies, percentages, means,

standard deviations, chi square, ‘t’ value and 'p' values were calculated.

‘t’ test was used to test the significance of difference between

quantitative variables and Yate’s and Fisher’s chi square tests for

qualitative variables. A 'p' value less than 0.05 is taken to denote

significant relationship.

91

DISCUSSION

In our study of 30 cases of Posterior Uveitis, it was observed that

posterior uveitis is more common in the age group of 26 to 35 years. Sex

incidence is almost equal in males and females. Unilateral and bilateral

cases are equal in ocurrence. Allof the cases were of chronic duration.

On analyzing the aetiology of posterior uveitis, in our study

majority of cases were found to be due to toxoplasmosis (43.3%),

followed by VKH syndrome (16.7%). Toxoplasmosis was the most

common infectious etiology found in our study.

Anatomical classification

In our study majority of cases were Retinochoroiditis (53.3%),

followed by Panuveitis (16.7%), Retinal vasculitis (13.3%),

Chorioretinitis (10%) and Choroiditis(6.7%).

Aetiological analysis

In our study, aetiological analysis of posterior uveitis showed that

majority of cases were of Toxoplasmosis(43.3%), followed by VKH

syndrome.

92

Retinal vasculitis with Systemic Lupus Erythematosus were

present in3 cases(females), 2 out of thatwere getting treatment at

Rheumatology department,Government General Hospital (GGH) with

systemic corticosteroids for the past 6 months with ANA anti ds DNA

antibody positivity. One case was presented to our hospital with

defective vision and Rheumatoogy workup done at rheumatology

department GGH, found to be ANA and anti ds DNA antibody

positivity and started on systemic corticosteroids.

3 cases were cytomegalovirus retinitis, out of that one case was

on treatment with anti retroviral drugs for the past 2 months in ART

centre with low CD4 count. Other 2 cases were presented to our institute

with defective vision and referred to ART centre for evaluation found to

be HIV positive with low CD4 levels and started on anti retroviral

therapy.

Tuberculous etiology was found in one case with quantiferon gold

positivity and sent to Thoracic medicine department at GGH for

evaluation and treated with antituberculous drugs and systemic

corticosteroids.

93

Clinical presentation

In our study, posterior uveitis is more common in age group of 26

– 35 years. Majority of cases of infectious posterior uveitis were

unilateral and non infectious posterior uveitis and panuveitis cases were

bilateral.

Complications

Since the main reason for poor visual outcomeis the structural

damage caused by the disease process, there is no significant visual

improvement even after the complete remission of the disease.

In our study cataract was present in 4 cases (13.3%), mainly in

cases of VKH syndrome.3 cases were presented with proliferative

retinopathy, 2 out of that were due to systemic lupus erythematosus with

retinal vasculitis, one was Eales disease.

Post inflammatory glaucoma was present in one case of VKH

syndrome. Subretinal fibrosis was present in one case and choroidal

neovascularization was present in another case of VKH syndrome.

Retinal detachment was present in one case of toxocariasis.

94

Treatment

In our study the most common drugs used for treatment is

systemic and topical corticosteroids followed by topical mydriatrics and

cycloplegics and anti toxoplasma agents.

Since all cases of posterior uveitis are of chronic in nature,

Immunomodulators are used in 11 cases (36.66%) as steroid sparing

agents in non infectious posterior uveitis and retinal vasculitis.

In our study, toxoplasmosis cases were treated with anti

toxoplasma agents and systemic corticosteroid. CMV retinitis patients

were treated with anti CMV agents. Serpiginous choriodopathy, SLE

with retinal vasculitis and Eales disease patients are treated with

systemic corticosteroid agents.

VKH patients were treated with topical corticosteroids, mydriatics

and cycloplegics, systemic corticosteroids and Immune modulators.

Immuno modulator therapy was given in VKH syndrome in Serpiginous

choroidopathy and SLE with retinal vasculitis.

Proliferative retinopathy cases were treated with Panretinal

photocoagulation, secondary glaucoma was treated with anti glaucoma

agents and choroidal neovascularization was treated with intra vitreal

95

bevacizumab.Since cataract was in early stage, without obstructing the

visual axis they were not treated.

Visual outcome

In our study, due to early diagnosis and prompt treatment the

disease was adequately controlled in all cases. But only 26.66% of

patients obtained significant visual improvement. Other 66.66% of

patients there is some visual improvement that is not very significant.

The main reason for poor visual outcome was chorioretinal atrophy in

the macula, the structural damage caused by the disease followed by the

complications namely sub retinal fibrosis and proliferative retinopathy.

In 6.6% of patients, there was no visual improvement due to

complications mainly choroidal neovascularization and tractional

retinal detachment. In choroidal neovascularization, after treatment

scarring was occurred but there was no visual improvement.

Out of 13 cases of Toxoplasmosis, 5 cases were involved the

extramacular area with good visual outcome and 8 cases were showed

macular involvement with less improvement in vision.

In VKH Syndrome, out of 5 cases 3 cases were improved vision

significantly . One case had subretinal fibrosis in macular area with

96

vision improving to 6/24. In one case vision was not improved due to

choroidal neovascularization.

In cytomegalovirus infection there was only mild improvement in

vision due to macular involvement. In serpiginous choroidopathy visual

outcome was affected by chorioretinal atrophy in macular area.

In Retinal vasculitis due to SLE and in Eales disease visual

outcome was affected by proliferative retinopathy. In tuberculosis vision

was improved significantly.

In Toxocariasis vision was not improved due to development of

tractional retinal detachment.

97

CONCLUSION

Posterior uveitis is a serious disease associated with vision

threatening complications.

Posterior uveitis is more common in the age group of 26-35

years.

All cases of posterior uveitis is of chronic duration.

All cases of posterior uveitis are severe in nature.

Retinochoroiditis is the most common anatomical type

comprising more than half of the cases.

Posterior uveitis due to infectious causes are common than non

infectious causes.

Toxoplasma is the most common aetiology detected in posterior

uveitis.

Toxoplasma is the major infectious aetiology found in posterior

uveitis.

98

In non infectious causes Vogt Koyanagi Harada syndrome,

vasculitis due to collagen vascular diseases are the common

causes.

With prompt treatment the disease is controlled in all cases of

posterior uveitis.

Corticosteroids are the most common drugs used for treatment of

posterior uveitis.

Immuno modulators are used as a steroid sparing agents in non

infectious posterior uveitis and retinal vasculitis.

Despite adequate control of the disease the visual outcome is

comparatively poor in posterior uveitis.

The main reason for poor visual prognosis is the structural

damage ( chorioretinal atrophy in the macula) caused by the

disease followed by complications.

In posterior uveitis visual prognosis depends upon the aetiology,

area of involvement and complications.

PART III

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200512000-00009

UVEITIS PROFORMA

Name : age/sex: date:

Phone no:

Occupation:

Address:

Complaints:

1) Symptoms of anterior segment involvement

Pain

Redness

Photophobia

2) floaters U/L, B/L

3) Defective vision-onset sudden / insidious

-painless / painful

h/o joint pain

trauma

surgery

history s/o focal sepsis ENT

Dental caries

h/o contact with TB/leprosy/ pet animals

h/o previous episodes

age at onset

no of episodes

response to treatment

h/o DM/ HT

h/o systemic diseases( rheumatoid arthritis& other connective tissue

disorders)

family history similar illness

Other significant history

Systemic examination

Pulse : /min BP : mmHg

Cardiovascular system:

Respiratory system:

Gastrointestinal system:

Central nervous system:

Ocular Examination

UCVA RE LE

BCVA RE LE

IOP RE LE

Slit lamp examination

Anterior segment RE LE

Lids edema

Conjunctiva ccc

Cornea- KPs fine/mutton

fat/pigmented

AC-

cells/flare/hypopyon/shallow

ac/Peripheral antrsynaechiae

Iris-CPN/atrophic patches/iris

bombe/koeppes/busaccas

nodules

Pupil-

RTL/RAPD/irregular/festooned

pupil/occulusiopupillae/seclusion

pupillae

Lens-posterior synaechiae/iris

pigment over lens/cataract

Anterior vitreous-cells/opacities

Fundus IDO

Fundus RE LE

Vitritis grade

I/II/III/IV

PVD

Choroidits patch-

yellowish ill defined

patch/atrophic

pigmented sharply

defined patch

Retinal edema

Sheathing of vessels

Disc edema

Retinal

hemorrhages

Cystoid macular

edema

Snowbanking/snow

ball opacities

Fundus diagram:RE LE:

Investigations

Fundus photo:

Hb

TC,DC,ESR,Mantouxtest,Chest X ray,RBS,Urinealb/sugar,VDRL/RA

factor/ACE/ANA factor and X ray sacro iliac joints

FFA:

B SCAN (if necessary):

TORCH screening

ENT opinion

Dental opinion

Rheumatology opinion

Chest physician opinion

Diagnosis - Acute/ Acute recurrent /Chronic

-Unilateral/Bilateral

-Posterior uveitis

-Aetiology

Treatment

Topical corticosteroids

Topical mydriatics and cycloplegics

Oral corticosteroids

Immunomodulators

Others :

Follow up

BCVA

Intraocular pressure

Healing of leisons

B SCAN (if necessary)

RE LE RE LE RE LE RE LE RE LE

1 Pradeep Kumar 25 / M DV RE -2 YrsDV LE x 1 WK

6/60 6/24 - Cells1+, Flare 1+ 1 4 1f 1d 1 1b 5,2, 1a, 1b 6/60 6/6

2 Rajan 36 / M DV BE x 1 WK 3/60 3/60 CCC, KP, Cell 2 + , Flare 2 + CCC, KP, Cell 2 + , Flare 2 + 2 2 2 2 2 2 1a, 1b, 2, 4 6/9 6/24

3 Kuppu 45 / F F, DV - RE x 1 Month 1/60 6/60 - - 3 1 6 N 3, 4 6 2, 6 6/36 6/60

4 Girirajan 37 / M DV BE x 2 Months 6/36 5/60 - - 1 1 3 3 2 3 2,4 6/24 6/36

5 Varalaxmi 36 / F F, DV LE x 1 Month 6/6 1/60 - Cells1+, Flare 1+ 1 4 N 1a 1 1a 2,5 6/6 6/36

6 Muniyammal 35 / F DV BE x 1 Month HM 4/60 - - 2 2 4b 4c 1, 6 4 10 3/60 6/60

7 Venkatesan 21 / M F, DV LE x 1 Month 6/6 6/24 - Cells1+, Flare 1+ 1 4 N 1d 1 1b 1a, 1b, 2, 5 6/6 6/12

8 Sridhar 30 / M F,DV RE 1 month 6/36 6/6 - - 4 1 1c N 1 1b 1a, 1b, 2, 5 6/12 6/6

9 Vijaya 30 / F DV BE x 2 Wks 6/60 HM CCC, KP + , Cells ++, Flare 2 +,PAS +,

CCC, KP +, Cells 2 +, Flare 2 + 2 2 2 2 2 2 1a,1b,2,3,4,9 6/24 6/12

10 Manikam 35 / M DV LE x 1 Wk 6/18 HM - - 1 6 8a 8b 2 8 2, 7 6/18 6/24

11 Rajesh 30 / M DV LE x 1 Month 6/6 3/60 - - 1 1 N 7 1 7 2 6/6 1/60

12 Vijayalakshmi 35 / F F, DV LE x 1 Month 6/6 6/36 - Cells1+, Flare 1+ 7 4 N 1c 1 1b 1a, 1b, 2, 5 6/6 6/12

13 Radha 38 / F DV LE x 2 Months 6/18 1/2 / 60 - - 7 2 - 4a 1, 6 4 10 6/18 4/60

14 Uma 25 / F F, DV RE x 2 Wks 1/60 6/6 Cells1+, Flare 1+ - 4 1 - 1c 1 1b 1a, 1b, 2, 5 6/12 6/6

15 Kathiresan 30 / M F, DV LE x 1 Month 1/2/60 6/6 - Cells1+, Flare 1+ 1 4 N 1a 1 1a 1a, 1b, 2, 5 6/60 6/6

16 Maheshwari 34 / F DV BE x 2 Wks 6/60 6/36 CCC, KP, Cell 2 + , Flare 2 + CCC, KP, Cell 2 + , Flare 2 + 2 2 2 2 2 2 1a, 1b, 2, 4 6/9 6/6

17 Susella 30 / F DV BE x 1 Month 3/60 2/60 - - - - 5 5 2,7 5 2,7 6/36 6/60

18 Kaniyappan 45 / M DV LE x 3 Months 6/18 HM - - - 2 N 4a 1, 6 4 10 6/18 3/60

19 Annamalai 40 / M DV BE x 2 Months 4/ 60 6/60 - - - - 3 3 2 3 2,4 6/24 6/36

20 Palani 29 / M DV BE x 2 Wks 4/60 4/60 CCC, KP +Cells 2 +, Flare 2 + , CCC +, KP +, Cells 2 +, Flare 2 + 2 2 2 2 2 2 1a, 1b, 2 ,4 6/9 6/9

21 Kumari 24 / F DV BE x 1 Month 3/60 4/60 - - - - 5 5 2, 7 5 2 6/36 6/24

22 Manivannan 31 / M F, DV RE x 1 Month 2/60 6/6 Cells1+, Flare 1+ - 4 1 1a N 1 1a 1a, 1b, 2, 5 6/36 6/6

23 Rangan 42 / M DV BE x 2 Months 6/60 6/36 ` - - - 3 3 2 3 2,4 6/36 6/12

24 Mariyammal 35 / F DV BE x 1 Wk 2/60 1/60 CCC, KP, Cell 2 + , Flare 2 + CCC +, KP +, Cells 2 +, Flare 2 + 2 2 2 2 2, 5 2 1a, 1b, 2, 4, 9 1/60 6/9

25 Vasantha 28 / F DV BE x 1 Month 6/60 4/60 - - - - 5 5 2, 7 5 2,7 6/60 6/36

26 Lakshmi 26 / F F, DV LE x 1 Wk 6/6 1/60 - Cells1+, Flare 1+ - 4 N 1a 1 1a 1a, 1b, 2, 5 6/6 4/60

27 Rajeswari 21 / F F, DV RE x 2 Wks 1/60 6/6 Cells1+, Flare 1+ - 4 - 1a - 1 1a 1a, 1b, 2, 5 6/6 6/36

28 Megala 28 / F F, DV LE x 2 Wks 6/6 2/60 - Cells1+, Flare 1+ - 4 N 1a 1 1a 1a, 1b, 2, 5 6/6 6/36

29 Sekar 34 / M F, DV RE x 2 Wks 1/60 6/6 Cells1+, Flare 1+ - 4 - 1a N 1 1a 1a, 1b, 2, 5 6/60 6/6

30 Ambiga 31 / F F, DV LE x 1 Month 6/6 1/60 - - - 4 N 1a 1 1a 1a, 1b, 2, 5 6/6 6/60

MASTER CHARTVISION

S.No NAME AGE/ SEX COMPLAINTS / DURATION

ANTERIOR SEGMENT VITREOUS FUNDUS FINAL VISION

INVESTIGATION DIAGNOSIS TREATMENT

KEY TO MASTER CHART

RE – Right eye

LE – Left eye

BE – Both eyes

F – Floaters

DV –Defective vision

CCC – Circum Corneal Congestion

Vitreous

1- Normal

2- Grade I vitreous haze

3- Grade II vitreous haze

4- Grade III vitreous haze

5- Grade IV vitreous haze

6- Vitreous haemorrhage

Fundus

1) 1a - Focal yellow white retinal lesion in the macula.

1b - Focal yellow white retinal lesion adjacent to pigmented

chorioretinal scar in the acula.

1c - Focal yellow white retinal lesion above supertemporal arcade

1d - Focal yellow white retinal lesion below supertemporal arcade

1e - Focal yellow white retinal lesion superior to macula and

below the supertemporal arcade.

1f - pigmented chorioretinal atrophic scar in the macula.

2 - Multiple serous retinal detachments with underlying choroidal

thickening and optic disc edema.

3 - Geographic yellow white subretinal patches with indistinct

margins from the disc running centrifugally extending to

posterior pole and macula.

4 4a- Dense white, well demarcated geographic areas of retinal

opacification associated with retinal hemorrhages in the

superotemporal arcade and macula.

4b - Dense white, well demarcated geographic areas of retinal

opacification associated with retinal hemorrhages in brushfire

like extension along the course of vascular arcade with

involvement of optic disc and macula.

4c - Granular opacification in the periphery.

5 5a - Cotton wool spots and flame shaped hemorrhages,hard

exudates in superotemporal and inferotemporal quadrant.

5b - Cotton wool spots and flame shaped hemorrhages,hard

exudates and neovascularization elsewhere in superotemporal

and inferotemporal quadrant

6 - Large solitary yellowish choroidal granuloma about 2 disc

diameters in size seen in inferonasal quadrant.

7 - Elevated white retinal lesion in superotemporal periphery

associated with fibrous band extending to macula.

8 8a - vitreous haemorrhage

8b - peripheral vascular sheathing in the supertemporal quadrant.

Diagnosis

1-Toxoplasmosis a) Macular area

b) Extramacular area

2- Vogt- Koyanagi- Harada Syndrome

3- Serpiginouschoroiditis

4- Cytomegalovirus retinitis

5- Systemic lupus erythematosus with retinal vasculitis

6- Tuberculosis

7- toxocariasis

8-Eales disease

Investigations

1- TORCH screening, Total Count, Differential Count, Erythrocyte

Sedimentation Rate

2- Fundus Fluorescein Angiography, RFT, LFT

3- chest x ray and Mantoux test

4- Quantiferon gold

5- Optical Coherence Tomography

6- Antinuclear antibody(ANA), anti double stranded DNA antibody(ds

DNA), Rheumatoid factor(RF) and anti neutrophil cytoplasmic

antibody (c ANCA, p ANCA)

Treatment

1- Topical corticosteroids, topical mydriatics and cycloplegics

2- Oral prednisolone

3- Intravenous Methyl prednisolone

4- immuomodulators

5- Anti Toxoplasma agents

6- Anti tubercular drugs

7- Panretinal photocoagulation

8- Intravitreal injection Bevacizumab

9- Antiglaucoma medications

10-Anticytomegalovirus drugs

ABBREVIATIONS

CMV - cytomegalovirus

VKH - Vogt Koyanagi Harada syndrome

IUSG - International Uveitis Study Group

ELISA - Enzyme Linked Immuno Sorbent Assay

TB - Tuberculosis

CNV - Choroidal neovascularization

SLE - Systemic lupus erythematosus

FFA - Fundus Fluorescein Angiography

RPE - Retinal Pigment Epithelium

HLA - Human Leucocyte Antigen

VDRL - Venereal Diseases Research Laboratory

RPR - Rapid Plasma Reagin

FTA- ABS - Fluorescent Treponemal Antibody Absorption test

HSV - Herpes Simplex Virus

VZV - Varicella Zoster Virus

HIV - Human immunodeficiency Virus

AIDS - Acquired Immunodeficiency Syndrome

CT - Computed Tomography

IOP - Intra Ocular Pressure

ATT - Anti Tubercular Therapy

TORCH - Toxoplasma

- Others

- Rubella

- Cytomegalovirus

- Herpes Simplex Virus

TC - Total Count

DC - Differential Count

ESR - Erythrocyte Sedimentation Rate

RFT - Renal Function Tests

LFT - Liver Function Tests

IDO - Indirect Ophthalmoscopy